Indirect surgical revascularization can be performed as part of complex aneurysm obliteration and moyamoya disease primarily in adults. There are several methods for establishing indirect revascularization, including multiple burr holes, encephaloduromyosynangiosis, and encephaloduroarteriosynangiosis/pial synangiosis, among others.

Creating burr multiple holes (Fig. 12.6) can promote neovascularization to the brain surface. On post-contrast images, enhancement across the burr holes can be appreciated and ADC maps can show increased diffusivity. Depending on the particular technique, favorable results are achieved in nearly 90% of cases. However, in some cases, the delicate anastomoses may not provide sufficient revascularization, and cerebral infarction may result as the underlying disease process ensues.

Encephaloduroarteriomyosynangiosis (EDAMS) consists of creating a linear craniotomy, narrow dural opening, and placing temporalis muscle flaps directly upon the exposed pial surface to stimulate collateral development (Fig. 12.7). The superficial temporal artery and attached flap are then sutured to the dura. Alternatively, encephalomyosynangiosis (EMS) can be performed for increasing both intracranial and extracranial collateral circulation by inserting the temporal muscle deep to the craniotomy flap directly upon surface of the brain. During the early postoperative period, the swollen muscle can exert mild mass effect upon the underlying brain parenchyma (Fig. 12.8). Postoperative angiography reveals good revascularization in the majority of cases.

Encephaloduroarteriosynangiosis (EDAS)/pial synangiosis consists of creating a defect in the dura and arachnoid to enable direct suturing of the superficial temporal artery to the pia (Fig. 12.9). Following successful synangiosis, angiography shows progressive reduced flow in the moyamoya vessels and increase in size of the superficial temporal artery.

Angiography is well suited for monitoring the effects of synangiosis. Indeed, the angiographic findings of synangiosis are characteristic and include early filling of the middle cerebral artery branches via ECA injection, enlargement of the superficial temporal artery and middle meningeal artery, and the presence of transpial or transdural collateral vessels. Progression of proximal MCA or ICA stenosis is often apparent despite a successful surgical and clinical outcome, presumably due to diverted blood flow through the ECA circulation. In fact, the lack of MCA or ICA stenosis is associated with a relatively poor outcome. CT and MRI can be used to assess for complications, which include recurrence of ischemic events and chronic subdural hematomas.

The concept of wrapping aneurysms with strips of muscle tissue was first introduced by Cushing as a treatment of ruptured aneurysms. The temporalis muscle is an accessible source of the necessary tissue. Alternatively, muslin has also been used as a wrapping material. Since the 1980s, the practice of wrapping aneurysms has declined in popularity. Nevertheless, muscle wrapping is still used as a last resort for treatment of aneurysms when endovascular stenting/embolization or surgical clipping is not feasible.

Following aneurysm wrapping surgery, the aneurysm will typically appear about the same size or perhaps slightly smaller, since the main goal of the procedure is to prevent further expansion. Although the muscle wrap itself is often inconspicuous, it should not be confused with tumor or other abnormalities, such as hemorrhage, on imaging (Fig. 12.10). However, the wrap can resorb and allow aneurysm expansion and bleeding. Other complications include infection or foreign body reaction, if synthetic materials are used. Thus, the role of imaging following aneurysm wrapping is to evaluate for integrity of the wrap, aneurysm expansion or hemorrhage, and abscess or muslinoma formation.

Aneurysm clips are used to occlude the neck of aneurysms in order to prevent or cease hemorrhage due to rupture. These devices are available in a variety of shapes and sizes. They consist of a hinged wire with parallel ends that are straight or curved. In the past, aneurysm clips were composed of stainless steel or tungsten. Although these materials are biocompatible, they are not MRI compatible. These clips also produce considerable beam-hardening artifact that can obscure surrounding structures. Newer clips are composed of non-ferromagnetic materials, such as titanium, which are MRI compatible and produce fewer artifacts on CT.

Surgery for aneurysm clipping consists of performing a craniotomy. In addition, variable amounts of the anterior clinoid process may be resected in order to access paraclinoid aneurysms (Fig. 12.11). Deeply positioned aneurysms can be difficult to attain for clipping, which can result in aneurysm remnants. Incomplete clipping can present as increased hemorrhage shortly after clipping of ruptured aneurysms, for example, and can be addressed by endovascular embolization (Fig. 12.12). Although the brain can be retracted in order to maximize the field of view and access for centrally located aneurysms, vascular injury can result. Likewise, vessels adjacent to aneurysms that have poor visibility can be inadvertently clipped, such as the recurrent artery of Heubner, which can result in caudate infarcts (Fig. 12.13).

Vasospasm is a significant source of morbidity in patients with ruptured cerebral aneurysms and typically manifests 7–10 days after the episode of subarachnoid hemorrhage. Transcranial Doppler ultrasound is routinely used to assess for cerebral vasospasm, but the modality has limited sensitivity and specificity. CTA is also commonly implemented for the detection of cerebral vasospasm following subarachnoid hemorrhage and may demonstrate multifocal steno-occlusive lesions and areas of hemorrhage (Fig. 12.14). In addition, CT perfusion can be performed concurrently to provide insight into the extent of cerebral ischemia resulting from vasospasm. Unfortunately, streak artifact from the aneurysm clip can limit the assessment of the adjacent vasculature. Ultimately, catheter-based angiography has been considered to be the historical gold standard to diagnose vasospasm.

The incidence of recurrent aneurysms after complete clipping is approximately is low, but this complication can lead to subarachnoid hemorrhage and requires repeat clipping or endovascular intervention. It is also important to carefully search for new aneurysms on postoperative scans, since the annual rate of de novo aneurysm formation is about 0.9%. These occur on average at about 10 years after surgery. Thus, long-term angiographic follow-up is warranted in patients with clipped aneurysms.

Microvascular decompression can be used to effectively treat vascular loop syndromes, such as trigeminal neuralgia and glossopharyngeal neuralgia (Figs. 12.19, 12.20, and 12.21). The technique essentially consists of interposing Teflon between the affected nerve and the offending vessel. The concept behind this procedure is that the Teflon distances and redirects the transmitted pulsation of the adjacent artery away from the nerve. Teflon is hyperattenuating on CT and low signal intensity on all MRI sequences. High-resolution T2-weighted MRI sequences are particularly useful for analyzing the position of the pledgets and altered anatomy, which often entails distortion of the nerve course. During the early postoperative period, reversible elevated T2 signal and restricted diffusion is often observed in the ipsilateral pons after trigeminal decompression and does not necessarily indicate infarction. Perhaps the most common complication of microvascular decompression is recurrent symptoms related to suboptimal pledget positioning (Fig. 12.22). For example, in patients with persistent hemifacial spasm after microvascular decompression, residual vascular compression is most commonly encountered proximal to the pledget, along the attached segment of the nerve. Hearing loss is a more unusual complication that can result from Teflon migration or the use of excess Teflon that compresses cranial nerve 8 within the internal auditory canal (Fig. 12.23). Granulomas can occasionally form in reaction to the presence of Teflon, which forms a mass that has low T2 signal and enhances (Fig. 12.24).

Carotid endarterectomy (CEA) is considered the treatment of choice for symptomatic and asymptomatic patients with high-grade carotid artery stenosis. In order to appropriately interpret imaging studies obtained following CEA, it is helpful to be familiar with the surgical techniques involved.

CEA can be performed through an incision made anterior to the sternocleidomastoid and ligation of the facial vein in order to expose the carotid bifurcation and clamping of the carotid artery distal to the endarterectomy. Consequently, a small hematoma within or adjacent to the sternocleidomastoid and mild circumferential narrowing of the carotid artery resulting from clamp placement during surgery can be appreciated on follow-up CT (Fig. 12.25). These findings are usually self-limited.

CEA involves opening the carotid artery, removing the plaque and associated endothelium, and suturing the vessel wall closed with or without an enlargement patch. The patch is usually composed of Dacron, which is not readily visible on CT, but can appear as a thin hyperechoic mesh on ultrasound (Fig. 12.26). Alternatively, the section of carotid artery that is resected can be reconstructed using a saphenous vein graft. This has a distinct patulous or bulbous appearance on imaging (Fig. 12.27).

Complications related to CEA include localized intimal flap or dissection, reperfusion syndrome, patch infection, restenosis, cerebral infarction, and cranial nerve injury, usually facial and hypoglossal (Figs. 12.28, 12.29, 12.30, 12.31, 12.32, and 12.33).

Hyperperfusion or reperfusion syndrome is an unusual complication of carotid endarterectomy or carotid artery stenting, occurring in 0.3–1.2% of cases. A possible etiology for this condition is impaired cerebrovascular autoregulation. Predisposing factors include severe underlying cerebrovascular disease, diabetes mellitus, long-standing hypertension, prolonged cross clamping during endarterectomy, and a greater than 100% increase in the degree of reestablished cerebral blood flow, which is usually associated with greater than 90% carotid artery stenosis. Patients may present with headaches, seizures, focal neurological deficits, or confusion within several days after surgery. Patients may recover completely if the diagnosis is made promptly. However, in some series, there is a mortality rate of up to 50%. The diagnosis of cerebral hyperperfusion syndrome can be suggested on CT in the proper setting by noting the presence of edema, often in the watershed zones ipsilateral to the side of surgery. On MRI, focal ipsilateral vasogenic edema is apparent. Diffusion-weighted imaging and apparent diffusion coefficient maps help confirm the presence of vasogenic edema. On MRA, prominent vessels on the affected side may be apparent. Similarly, perfusion-weighted imaging can depict the relative increased flow to the affected side. The finding of hemorrhage portends a poor prognosis. Imaging can help identify hyperperfusion syndrome before serious sequelae result. Differential considerations for the imaging appearance of cerebral hyperperfusion syndrome include hypertensive encephalopathy, cyclosporine toxicity, and eclampsia. The lack of restricted diffusion helps exclude cerebral ischemia.

Recurrent stenosis after carotid endarterectomy occurs at the rate of about 1% per year. This complication is the main limitation of carotid endarterectomy and predisposes to cerebrovascular ischemia. Acute thrombotic occlusion is much less common and is a potentially devastating complication that can result in cerebral infection. Conventional carotid endarterectomy with patch angioplasty and the use of lipid-lowering pharmaceuticals are associated with lower rates of restenosis. Risk factors for restenosis include female gender and renal failure. CTA, MRA, and Doppler ultrasound are all appropriate for evaluation of suspected restenosis or occlusion after carotid endarterectomy. Each of these modalities has advantages and disadvantages. CTA with reformats, especially the curved planar reformats, is useful for studying stenoses. In the setting of carotid endarterectomy with patching, the internal carotid artery velocities on Doppler ultrasound must be interpreted with caution, since these are normally higher than in the nonoperated counterparts. MRA is best suited for identifying pseudo-occlusions.

Electrical stimulation of the carotid sinus can be used to treat systemic hypertension that is unresponsive to medical therapy. The phenomenon is effectuated by initiating the baroreceptor reflex and decreasing sympathetic tone. Implanted carotid sinus stimulation systems comprise a pulse generator and bilateral perivascular carotid sinus leads (Fig. 12.34). Insertion of these devices does not appear to cause carotid artery injury or other major side effects.

Adjustable vascular clamps were first introduced in the 1950s for treating carotid system aneurysms. Several varieties of metallic extracranial carotid vascular clamps have been developed, including the Selverstone, Crutchfield, Poppen-Blaylock, Salibi, and Kindt. The principle behind such vascular clamps is to reduce blood flow and to promote clotting of the aneurysm. If collateral circulation via the circle of Willis is inadequate, the clamps can be loosened. Gradual, graded occlusion of the carotids would yield better results than immediate occlusion. Over time, however, carotid revascularization can occur through the clamp and regular follow-up is recommended. On imaging, the clamps are recognized as rectangle-shaped metallic parts with central openings of variable sizes (Fig. 12.35). The lumen distal to the clamp becomes diffusely narrowed and usually remains as such even after the clamp is removed.

Reconstruction of the great vessels may be performed for treatment of steno-occlusive lesions of congenital aberrations. The surgical maneuvers can be complicated and involve reimplantation of normal vessels onto others (Fig. 12.36) and/or the use of bypass grafts, such as collagen-impregnated Dacron and polytetrafluoroethylene (Figs. 12.37 and 12.38), each with different imaging appearing. Postoperative MRA, CTA, Doppler ultrasound, or catheter angiography can be used to evaluate suspected restenosis or occlusion (Fig. 12.39).

Endovascular cerebrovascular procedures include endovascular reconstruction or deconstruction for cerebrovascular occlusive disease or active bleeding using stents or embolic material; embolization of tumors, aneurysms, or vascular malformations either preoperatively or for treatment; and mechanical or chemical thrombolysis for acute ischemic stroke or vasospasm. Materials that are typically used during neuroendovascular procedures include metal containing devices, such as coils, plugs, and stents, liquid embolic agents, balloons, and particles. Certain metals contained in some of these endovascular treatment modalities create substantial streak artifact on CT, rendering imaging less sensitive to vascular assessment. Most intracranial endovascular devices create relatively less artifact on MRI compared to CT. For example, embolic coils used in aneurysm are predominantly made of platinum. These have only mild susceptibility effect on MRI/MRA. Indeed, MRA is an effective means to assess small degrees of aneurysm recurrence following coil embolization (Fig. 12.40). Most intracranial stents have relatively low mass, but still produce susceptibility artifacts on MRI, giving the corresponding vessel’s intraluminal diameter a false appearance of being narrowed (Fig. 12.41). Liquid embolic agents, such as Onyx, generally produce a signal void on MRA, T1-, and T2-weighted MRI without significant obscuration of adjacent vasculature (Fig. 12.42). However, Onyx HD500 used for treating aneurysms is associated with more susceptibility effect compared to Onyx used for arteriovenous malformation embolization, which can overestimate the degree of stenosis on MRA (Fig. 12.43).